(Reduced risk for dementia)
Neurodegenerative disorders are chronic conditions that result from accumulated injury and damage to parts of the brain. These conditions typically have a gradual onset and manifest later in life. Many will prove to be fatal or at least contributory to the person’s ultimate death. We have long attributed them to the consequences of the aging process; in small or large part, depending upon the specific disorder, likely contributed to due to predisposition by virtue of gene mutations though except in certain conditions, such as Huntington disease, inadequately identified or understood and likely to be complex; and impacted by environmental exposures (alcohol being a very significant one).[1] There has been mounting evidence over the past decade that healthy ageing may be important to lowering dementia risk that is a feature of a number of neurodegenerative disorders, with modifiable risk factors including blood pressure, body fat percentage and exercise. However, more recently, evidence for the role of neuroinflammation (inflammation in the brain) is gaining a growing consensus as a pathophysiologic factor in neurocognitive decline and eventual dementia, as well as playing a role in some specific neurodegenerative conditions, and viruses are being implicated as significant actors in causing neuroinflammation.[2] There are now 45 significant associations in longitudinal data with respect to prior viral infection and subsequent development of a neurodegenerative disorder. (see reference 5).
Neurodegenerative disorders are a matter of significant public health concern due to their increasing prevalence; expected continued increase in the future; the significant health risks, disability and costs that result; and the burden on family members that results in caring for these family members.
There are many specific diseases that are included under the classification of neurodegenerative disorders, and I will not list them all, but here is a framework developed by the Cleveland Clinic[3] that I find helpful in which to think about them and I will list some representative conditions:
- Dementia-type diseases – these are neurodegenerative diseases in which dementia is the predominant manifestation of the disease
- Alzheimer’s disease (AD)
- Frontotemporal dementia
- Lewy body dementia
- Chronic traumatic encephalopathy (CTE)
- Demyelinating diseases – these diseases are characterized by damage to and loss of the myelin sheath that surrounds and insulates nerve cells, both protecting the cells, but also providing insulation that aids in the transmission of signals from one cell to another.
- Multiple sclerosis (MS)
- Neuromyelitis optica spectrum disorder
- Parkinson’s and Parkinson’s-like diseases – these are movement disorders often characterized by stiffness, rigidity, tremors, and slowed movements
- Parkinson’s disease (PD)
- Normal pressure hydrocephalus
- Wilson’s disease
- Multiple system atrophy
- Corticobasal degeneration
- Drug-induced parkinsonism
- Motor neuron diseases – these are diseases that destroy the neurons that are responsible for strength and movement
- Amyotrophic lateral sclerosis (ALS or Lou Gehrig’s disease)
- Progressive supranuclear palsy
- Prion diseases – these are diseases that result from “infectious” proteins that cause brain impairment due to abnormal folding and function of the proteins (most people are more familiar with these diseases in animals, e.g., “mad cow disease” in cattle and chronic wasting disease in deer and elk).
- Creutzfeldt-Jakob disease
Some viruses may be able to get to and infect neurons in the brain to cause inflammation and damage, while others are more likely to produce injury indirectly through the response of supporting cells adjacent to neurons such as astrocytes and microglial cells or the in-migration of immune cells that have received signals resulting from the detection of virus in the body. Further, those viruses that can cause persistent infection and therefore long-term chronic inflammation or those that can undergo reactivation with other infections or immunosuppression are of special concern, including those that may result in autoreactive immune responses that damage neurons. Autoimmunity has recently been implicated as potentially having a role in the development of ALS. In AD, beta-amyloid and tau protein deposition and accumulation have been implicated in the damage to neurons that can then result in this disease. It appears that these proteins can be deposited as part of the neurological response to inflammation and/or infection of neurons. In some cases, severe infections (and this was clearly shown for COVID-19) can lead to brain atrophy (shrinkage) and loss of brain volume.
Herpes viruses have a particular affinity for neurons and have been known for some time to infect brain cells resulting in encephalitis, seizures and other neurological manifestations in some individuals. Herpes viruses are also typically life-long infections and the viruses are known for their ability to reactivate with stress, other infection or immunosuppression. This group of viruses includes herpes simplex virus – 1 (HSV1) and it appears that this infection can increase the risk for AD (patients whose blood tests evidenced past infection were at higher risk for AD and the DNA from this virus has been discovered in beta-amyloid plaques in patients with AD). The risk for AD was highest in those with a history of viral encephalitis.
Epstein-Barr Virus infection (infectious mononucleosis) has been identified as a significant risk factor (risk increased by a factor of roughly 32) and trigger for the subsequent development of MS, more so in those who had symptomatic infection.
Influenza and herpesviruses can trigger acute or chronic Parkinson-like symptoms or can result in post-encephalitic parkinsonism. Of note, a huge increase in post-encephalitic parkinsonism was noted following the Spanish flu pandemic of 1918-19.
A very recent study has revealed insights that an otherwise innocuous human virus may precipitate Parkinson’s disease in those with certain genetic risk factors.[4]
The good news is that four vaccines have now been shown to reduce the risk for dementia, and certainly when you understand what I have shared above, it makes sense. Here they are:
- The influenza vaccine[5]
The investigators showed that influenza with pneumonia was associated with a significant increase in risk for later development of AD, PD, ALS, and dementia. This increased risk can persist for 15 years or more. Given the ability of influenza vaccine to reduce infections, and particularly, severe disease, it is not surprising that influenza vaccination is associated with reduced chances for the development of AD and dementia.[6] That study showed that adults over age 65 who received a flu vaccine were about 40 percent less likely to develop Alzheimer’s. A 2024 study showed that adults who received the flu vaccine had a 21 percent lower chance of developing AD and a 42 percent reduction in the risk of developing vascular dementia.[7]
- The RSV vaccine
Although the RSV vaccine for adults was only recently made available, a study published this year was already able to demonstrate a reduced risk of dementia over a period of 18 months following RSV vaccine that was above and beyond the reduction achieved compared to those who only received the influenza vaccine.[8]
- The Shingles (Zostavax) vaccine
Researchers found that those adults who received the shingles vaccine were 20 percent less likely to develop dementia within the next seven years compared to those who did not receive this vaccine, and the benefit was even greater for women.[9]
- Tdap (Tetanus, diphtheria, and acellular pertussis)
A 2021 study showed that among adults over age 65, those who received both the shingles vaccine and the Tdap vaccine had a 42 to 50 percent lower risk of developing dementia compared to those who got no vaccines.[10] Receiving even just the shingles vaccine or just the Tdap was associated with 25% and 18% reductions in risk for dementia, respectively.
There is growing evidence that the beneficial effect of these vaccines is not limited to disease prevention for which the vaccines are intended, but that there is an additional anti-inflammatory benefit from the vaccine ingredients themselves. This is somewhat supported in that some studies have also demonstrated diminished rates of stroke and heart attack following vaccination. We know from our COVID-19 studies that the risks of heart attack and stroke appear to be doubled for a year or more following COVID-19. Unfortunately, with antivaccine disinformation gaining ground steadily, fewer seniors are getting these vaccines, and unfortunately, many of these victims of disinformation will be the ones to pay the price.
[1] Associations of environmental factors with neurodegeneration: An exposome-wide Mendelian randomization investigation, Li, D., Zhou, L. et al., Ageing Research Reviews, Volume 95, 2024, 102254, ISSN 1568-1637, https://doi.org/10.1016/j.arr.2024.102254.
[2] Viruses in neurodegenerative diseases: More than just suspects in crimes. Leblanc P, Vorberg IM. PLoS Pathog. 2022 Aug 4;18(8):e1010670. https://pmc.ncbi.nlm.nih.gov/articles/PMC9352104/.
[3] https://my.clevelandclinic.org/health/diseases/24976-neurodegenerative-diseases.
[4] Human pegivirus alters brain and blood immune and transcriptomic profiles of patients with Parkinson’s disease, Hanson, B., Dang, X, et al. JCI Insight. July 2025. https://insight.jci.org/articles/view/189988.
[5] Virus exposure and neurodegenerative disease risk across national biobanks, Levine, K, Leonard, H., et al. Neuron, volume 111, issue 7, p1086-1093.e2, April 05, 2023.
[6] Risk of Alzheimer’s disease following influenza vaccination: a claims-based cohort study using propensity score matching, Bukhbinder, A.S., Ling, Y. et al, J. Alzheimers Dis. 2022; 88:1061-1074.
[7] Prospective cohort study evaluating the association between influenza vaccination and neurodegenerative diseases. Zhao, H., Zhou, X., et al. npj Vaccines 9, 51 (2024). https://doi.org/10.1038/s41541-024-00841-z.
[8] Lower risk of dementia with AS01-adjuvanted vaccination against shingles and respiratory syncytial virus infections. Taquet, M., Todd, J.A. & Harrison, P.J., npj Vaccines 10, 130 (2025). https://doi.org/10.1038/s41541-025-01172-3.
[9] A natural experiment on the effect of herpes zoster vaccination on dementia. Eyting, M., Xie, M. et al. Nature 641, 438–446 (2025). https://doi.org/10.1038/s41586-025-08800-x.
[10] Comparison of rates of dementia among older adult recipients of two, one, or no vaccinations. Wiemken TL, Salas J, et al, J Am Geriatr Soc. 2022; 70(4): 1157-1168. doi:10.1111/jgs.17606.
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